Prevent brain ageing with personalised nutrigenomics Prof. Michael Fenech University of South Australia: Michael.Fenech@unisa.edu.au Genome Health Foundation: mf.ghf@outlook.com
Healthy Neuron Tau tangles Diseased Neuron Amyloid plaques Alzheimer's Disease Progression, Courtesy of American Health Assistance Foundation
? PRECLINICAL MILD COGNITIVE ALZHEIMER’S APPARENTLY NORMAL IMPAIRMENT Silent phase: brain changes Cognitive changes are of Impairment in two or more without obvious cognitive concern to individual and cognitive functions. impairment family but impairment does Cognitive impairment severe Individual notices some not interfere with activities of enough to cause inability to symptoms but not detectable daily living perform daily living tasks by tests OPPORTUNITY TO INTERVENE NUTRITIONALLY TO TOO LATE STALL OR REVERSE COGNITIVE IMPAIRMENT IRREVERSIBLE
Nutrient intake and brain biomarkers of Alzheimer’s disease in at-risk cognitively normal individuals: Cross-sectional neuroimaging pilot study GLUCOSE UPTAKE METABOLISM FDG-PET Control naMCI aMCI AD PIB-PET AMYLOID Higher dietary intake of folate and β-carotene associated with more brain glucose use (FDG SUVR) Higher dietary intake of vit D, vit B12 and EPA associated with less brain amyloid (PIB SUVR)
HOMOCYSTEINE LOWERING BY B VITAMINS SLOWS BRAIN ATROPHY AND COGNITIVE DECLINE IN MILD COGNITIVE IMPAIRMENT VITACOG PLACEBO-CONTROLLED TRIAL 2y FOLIC ACID [0.8 mg/d], B12 [0.5 mg/d] B6 [20mg/d] Amnestic or non-amnestic MCI, >70y PLACEBO ACTIVE Key points B vits for 2 years slows cognitive • decline and brain atrophy in MCI These benefits are mainly found • in those with plasma homocysteine >11umol/L • Effects mainly attributable to B12 Smith AD et al 2010 Plos One, deJager CA et al Int J Ger Psych 2012, Douaud et al PNAS 2013
EFFECT OF COMBINED B6, B9, B12 SUPPLEMENTATION ON PREVENTION OF BRAIN ATROPHY AND COGNITIVE FUNCTION IN CASES OF MILD COGNITIVE IMPAIRMENT DEPENDS ON OMEGA-3 STATUS Placebo B vitamins It is important to identify susceptible sub-groups when designing clinical trials. Only those with plasma Homocysteine >11μmol/L and/or plasma Omega-3 fatty acids >390μmol/L benefited from B6+B9+B12 supplementation Jerneren et al Am J Clin Nutr 2015, 102:215-221 Oulhaj A et al J Alz Dis 2016, 50:547-557
ALZHEIMER’S RISK GENES
Significant MMSE and B-12 X APOEε4 interaction B-12 X APOε4 interactions Were also observed for Digit span and RAVLT neuropsych tests Better performance in MMSE, Digit span and RAVLT tests was associated with vitamin B-12 in APOE e4 carriers but not in APOE e4 non- carriers. Tze-Pin Ng et al
B12 STATUS X APOE GENOTYPE INTERACTION AND COGNITIVE FUNCTION Evidence for APOEε4 x Vit B-12 interaction on cognitive function is increasing supporting the hypothesis that intervention with B-12 may prove to more beneficial in APOEε4 carriers Population-based study of 1935 participants, aged 71 to 74 years Vogiatzoglou et al 2013 Psychosomatic Med Vol 75
TAKE HOME MESSAGES • Brain ageing starts to accelerate from age 30 onwards • Adopt a diet rich in carotenoids, folate, vitamin D, vitamin B12 and omega-3 fatty acids (i.e. fruit, veg, fish) • Eat oily fish which are rich in vitamin B12, vitamin D and omega-3 fatty acids Your risk for Alzheimer’s disease is much higher if you are a carrier of the ancestral APOE ɛ4 mutation • APOE ɛ4 mutation carriers may be more susceptible to the brain ageing effects of vitamin B12 deficiency. • APOE ɛ4 carriers also benefit more from aerobic exercise with regards to cognitive function. • In the near future an “avatar” for each person may be available to optimise lifestyle therapy to prevent dementia. • See your doctor and improve your diet and life-style as soon as you start to experience cognitive impairment •
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